Proper diagnosis, care may allow some patients to return to sports participation

ANAHEIM, Calif. — Various studies and guidelines have been published to assist cardiologists in the diagnosis and appropriate treatment of patients who participate in sports, according to diagnosing conditions, treating patients and recommending participation, according to presentations at the American Heart Association Scientific Sessions.

ECG Criteria

Most cardiologists are inclined to use the most recent ECG criteria, which is the international recommendations that have been published in the British Journal of Sports Medicine, Journal of the American College of Cardiology and the European Heart Journal, Eugene H. Chung, MD, FHRS, FAHA, associate professor of internal medicine, director of the West Michigan Program cardiac electrophysiology service and director of the sports cardiology clinic at the University of Michigan in Ann Arbor, said in a presentation. These guidelines define an athlete as someone who is between the age of 12 years and 35 years, engaged in regular exercise or training and has no known inherited condition.

The recommendations recognize variances in the ECG that may be seen based on sex, ethnicity, age, conditioning and type of sport, as well as the increased prevalence of other comorbidities in patients older than 35 years. Once the ECG is read, it can be considered normal, borderline or abnormal, which then determines whether further evaluation is needed.

“That document was the result of many years of hard labor, hard work and refinement over the last 20 or so years,” Chung said.

The progress started with a document on screening for hypertrophic cardiomyopathy in young athletes, which was published in The New England Journal of Medicine in 1998. In this Italian study, there was a very low prevalence of hypertrophic cardiomyopathy (3%), although around 38% had an abnormal ECG.

In a study published in Circulation in 2000, researchers found that 40% of athletes had abnormal ECGs using the same criteria as the 1998 study.

The unacceptably high rate of abnormal ECGs resulted in the first consensus document in 2005 from the European Society of Cardiology, which listed what abnormalities to look for in ECGs of young competitive athletes.

In a study using the 2005 ESC guidelines published in the Annals of Internal Medicine in 2010, adding ECG to physical examination and medical history improved overall sensitivity and decreased the false-positive rate to 16.9%, Chung said.

Various studies including one published in HeartRhythm in 2011 confirmed that the false positive rate was still high (19%) when using the European Society of Cardiology 2005 guidelines.

These studies resulted in a 2010 version of the European Society of Cardiology guidelines.

“This for the first time identified a group 1, or normal, and a group 2, uncommon or abnormal, categorization of ECG findings” Chung said.

Through these updated guidelines, specificity was improved, as shown in a study published in Heart in 2011.

It was later found that about half of the ECGs that were considered abnormal were caused by left axis deviation or left anterior hemiblock, left atrial enlargement, right ventricular hypertrophy or right axis deviation or left posterior hemiblock.

The Seattle Criteria were published in 2012, which reflected results from previous studies that focused on the European Society of Cardiology 2010 guidelines. These new guidelines reduced the number of positive ECGs, according to a study published in Circulation in 2014.

“However, we still have room to improve, especially in the African-American athletes,” Chung said.

Studies since these guidelines were released found that early repolarization in the anterior precordial leads associated with inverted T-waves are common in black individuals.

These studies led to the next version of the guidelines, the Refined Criteria, which introduced a borderline variant group that included left atrial enlargement, axis deviation, right ventricular hypertrophy and T-wave inversions in black athletes.

The international recommendations were a result of the Summit on ECG Interpretation in Athletes in 2015. Some major changes included further modifications regarding findings such as left ventricular hypertrophy, left atrial enlargement and right ventricular hypertrophy. A few parts of the criteria that were once abnormal were now normal, according to the presentation.

“A very important part of the document is that some detailed recommendations are given about working up ECG abnormalities,” Chung said.

A study published in the Journal of the American College of Cardiology in 2017 compared the new guidelines  with ones that had been previously published. The number of positive ECGs decreased with the international recommendations.

“Despite the improvement of the positive rate, we still have work to do,” Chung said. “There’s quite an overlap between [hypertrophic cardiomyopathy] and [arrhythmogenic right ventricular cardiomyopathy] with an athletic heart regarding voltage and T-wave inversions.”

Some research has been done over the years on T-wave inversion, hypertrophic cardiomyopathy and the Brugada pattern, which may help develop future guidelines.

More research needs to be conducted on different ethnic populations, mixed race individuals, adolescent athletes and lifelong or masters athletes, in addition to the continued refinement of the guidelines, according to the presentation.

Treating athletic patients

A document has recently been published in the Journal of the American College of Cardiology on the treatment of athletes or highly active people.

“It was intended to put together a core curriculum for practicing sports cardiology,” Aaron L. Baggish, MD, FACC, FACSM, associate professor of medicine at Harvard Medical School and director of the Cardiovascular Performance Program at Massachusetts General Hospital, said in the presentation. “It was really designed for the clinician in the trenches as a resource to turn to when thinking about how best to take care of the athletic patient.”

Four pillars were laid out in the document regarding comprehensive sports cardiology, including differentiation of exercise-induced cardiac remodeling from CV pathology, evaluation of the symptomatic competitive athletes and highly active people, management of those patients with CVD and collaborative preparticipation CV screening.

Although syncope is a major form of collapse for athletic patients, there are other causes, including heat stroke, seizure, cardiac arrest, hyponatremia and exercise-associated collapse. There are two forms of syncope: neural and cardiac.

“Clearly as cardiologists, our job is to evaluate and to find the causes of cardiac syncope, which are typically in athletes caused by tachyarrhythmias, but far more common than cardiac arrhythmia-related syncope or neutrally-mediated syncope, and perhaps the one that deserves the most attention because this is one that we see most commonly in the context of athletic participation is post-exertional syncope,” Baggish said.

The measurement of an increased heart rate shows that endurance exercise is an extreme state of vasodilation, according to the presentation.

For post-exertional syncope, the intervention is raising the athlete’s legs, not CPR.

This does not happen all the time because when athletes stop exercising, they often maintain posture. This helps to move venous blood out of the lower extremities and into thorax, which is then shifted into the brain. If an athlete stops immediately and uses something to stabilize their body weight, this can lead to post-exertional collapse.

Some interventions that may help with post-exertional hypotension include drinking water, adding salt to a meal before exercise, compression socks, walking after running, sleep and the use of oral contraceptives, according to the presentation.

Examining a patient who had syncope is an important step.

“The evaluation syncope rests on careful, detailed medical history,” Baggish said.

Videos of athletes during the episode may help cardiologists treat patients. ECG, diagnostic imaging and exercise testing is also helpful, according to the presentation.

Chest pain is another common diagnosis in athletes. Non-cardiac causes of chest pain are the most common, and a cardiac etiology of chest pain occur in 5% to 10% of patients.

“The issue is that cardiac causes kill,” Baggish said.

Age dictates the differential with a cutoff point of 35 years old, according to the presentation. Chest pain occurs in the younger patient one in every 500 to 700 cases, and anatomy dictates risk. Symptoms are common, but are not those of typical anginal chest pain. ECGs are of limited value, and exercise tests are often false. If an anomalous coronary artery is suspected, imaging is suggested. Medical history and exercise tests are also helpful in diagnosing chest pain.

Palpitations are a symptom, not a diagnosis, according to the presentation. Those that are unrelated to exercise are common and often benign, and palpitations related to exercise are considered pathology unless proven otherwise through diagnostic testing. Managing patients with palpitations starts with ECGs and medical history.

Palpitations may also be a result of substance use or abuse and may include methylphenidate, cocaine, over-to-counter stimulants, alcohol and growth hormones.

“If we don’t ask our patients about this, we’ll never hear about it,” Baggish said.

Exercise recommendations

Family cascade screening for channelopathies and cardiomyopathies is important, especially in patients who may carry a pathogenic gene but who do not express the disease.

“For this reason, we’re going to be seeing more and more of these phenotype-negative patients in our practices,” Rachel J. Lampert, MD, professor of internal medicine (cardiology) at Yale University School of Medicine, said in the presentation. Carrying a gene while not expressing the disease carries different implications for different diseases.

The progression of arrhythmogenic right ventricular cardiomyopathy may be accelerated through exercise, according to the presentation. Exercise impacts the left and right ventricle with increased wall stress in the right ventricle.

“This in turn can potentially worsen RV dysfunction if the RV is abnormal,” Lampert said.

Exercise is not recommended for patients with arrhythmogenic right ventricular cardiomyopathy, according to the American Heart Association/American College of Cardiology scientific statement published in Circulation in 2015.

“That document does not address the phenotype-negative patient other than to recommend continued follow-up,” Lampert said. “However, the ARVC disease-specific guidelines also from 2015 do state the restriction from competitive sports should be considered for healthy gene carriers.”

A major question that persists is how much exercise is safe for carriers of the arrhythmogenic right ventricular cardiomyopathy mutation. Some studies found that recreational sports are not harmful, while others suggest any athletic participation beyond the AHA recommended minimum may be detrimental.

“This is an important question that so many ARVC patients really want to know the answer to,” Lampert said. “We know they can’t do endurance exercise, but for the swimmer, for example, is it five, 10, 20, how many laps is it?”

It has been suggested that exercise is not ideal for patients with hypertrophic cardiomyopathy expression and may lead to small vessel ischemia and increased fibrosis, although some studies have found exercise to have an opposite effect. In a study published in Circulation Research in 2006, exercise prevented fibrosis, improved markers of hypertrophy and prevented myocyte disarray in a mouse model.

“This is just one mutation, and we can’t extrapolate directly to people from a single mouse model, but I think it’s certainly interesting and provocative data,” Lampert said.

Other studies have found that moderate intensity exercise training may improve peak oxygen consumption and resulted in no arrhythmias. Echocardiographic parameters did not change throughout this study. Exercise may also improve diastolic and endothelial function in patients with HF with preserved ejection fraction, according to the presentation.

The AHA/ACC document does not recommend restricting competitive exercise in these phenotype negative hypertrophic cardiomyopathy patients, even in the absence of data, although the European guidelines does recommend restricting patients who are phenotype-negative.

The qualification of a phenotype-negative patient is less helpful for those with long QT syndrome, according to the presentation, as manifestation of QT prolongation can vary from day to day. Treating patients who are genotype-positive for long QT syndrome who are asymptomatic is similar to that for asymptomatic, but manifest long QT syndrome. This includes avoiding QT-prolonging drugs and electrolyte abnormalities and treating with beta-blockers.

 

In several studies, no adverse events were seen in patients with long QT syndrome who continued sports after appropriate treatment.

Sports may be considered for patients with genotype-positive/phenotype-negative long QT syndrome who are asymptomatic to participate in sports, according to the recommendations published in Circulation in 2015.

For patients with catecholaminergic polymorphic ventricular tachycardia, exercise is not recommended. Catecholamines increase arrhythmias, and patients in some studies with the condition who have ICDs have died from inappropriate shocks. Referring these patients with CVD to a specialty center is recommended if return-to-play is considered.

In general, since 2005, recommendations have changed from a yes-no approach to more of a class and level of evidence approach. It has also been recognized that patients can participate in their own decisions and should be involved in shared decision-making with their physicians.

“The phrase ‘shared decision-making’ does not appear in the 2015 eligibility guidelines, but it’s inherent in the use of class II recommendations, that is, return to play may be reasonable, may be considered vs. the prior yes-no,” Lampert said. – by Darlene Dobkowski

Reference:

Chung EH,

Baggish AL,

Lampert RJ. Screening and Managing Athletes with Sudden Cardiac Death Risk. All presented at: American Heart Association Scientific Sessions; Nov. 11-15, 2017; Anaheim, Calif.

Ackerman MJ, et al. Circulation. 2015;doi:10.1161/CIR.0000000000000246.

Baggish AL, et al. Ann Intern Med. 2010;doi:10.7326/0003-4819-152-5-201003020-00004.

Baggish AL, et al. J Am Coll Cardiol. 2017;doi: 10.1016/j.jacc.2017.08.055.

Corrado D, et al. N Engl J Med. 1998;doi:10.1056/NEJM199808063390602.

Dhutia H, et al. J Am Coll Cardiol. 2017;doi:10.1016/j.jacc.2017.06.018.

Konhilas JP, et al. Circ Res. 2006;doi:10.1161/01.RES.0000205766.97556.00.

Malhotra R, et al. HeartRhythm. 2011;doi:10.1016/j.hrthm.2010.12.024.

Maron BJ, et al. Circulation. 2015;doi:10.1161/CIR.0000000000000239.

Pelliccia A, et al. Circulation. 2000;doi:10.1161/01.CIR.102.3.278.

Sheikh N, et al. Circulation. 2014;doi:10.1161/CIRCULATIONAHA.113.006179.

Weiner RB, et al. Heart. 2011;doi:10.1136/hrt.2011.227330.

Disclosure : Baggish reports he receives funding from the American Heart Association, American Society of Echocardiography, Department of Defense, the National Football League Players Association and the NIH, and has numerous athletic affiliations. Chung reports no relevant financial disclosures. Lampert reports she received research funding from and participated in clinical trials for Boston Scientific/Guidant, Medtronic and St. Jude Medical and honoraria/consulting fees from Boston Scientific/Guidant and Medtronic.